These data indicate that moderate weight loss during long-term calorie restriction is associated with a marked clinical improvement which reflects the reduction in insulin concentrations and reciprocal changes in SHBG. The improvement in menstrual function and fertility may therefore be consequent upon an increase in insulin sensitivity which, directly or indirectly, affects ovarian function.

We postulate that PCO and male pattern baldness are caused by alleles of the same gene which affect androgen production or action. The different frequencies of PCO and male pattern baldness arise from differing thresholds for phenotypic expression in females and males respectively. The modifying effects of other genes is the most likely explanation of the somewhat variable phenotype.

OBJECTIVE Polycystic ovary syndrome is one of the most common endocrine disorders but its aetiology remains unknown. It is highly prevalent within families, suggesting a genetic basic for the syndrome, but the mode of inheritance is unclear. The purpose of this study was to determine the mode of inheritance of polycystic ovary syndrome, within the families of affected individuals, by classic segregation analysis. DESIGN All first degree relatives of affected individuals were screened for the presence or absence of polycystic ovaries in post-menarchal-premenopausal women and early onset male pattern baldness (MPB) in the males. In extended pedigrees, assignment of affected status in postmenopausal women was made by consideration of the clinical history alone. PATIENTS Fourteen women (probands), presenting with a variety of clinical symptoms, were identified sequentially as having polycystic ovaries (PCO) by ultrasound scan. They were examined in detail to determine their family structure, clinical and endocrine status. Ten families were found to have sufficient members for further study. MEASUREMENTS All family members had their body mass index calculated, their degree of hirsutism assessed using the Ferriman and Gallwey score and serum levels of gonadotrophins (FSH and LH), testosterone, prolactin and 17a-hydroxyprogesterone measured by radioimmunoassay. A careful reproductive history was taken for each woman and any menstrual disturbance was noted. Obese probands had their glucose and insulin response to a standard 75-9 oral glucose tolerance test determined.Each male family member was also assessed for the degree and time of onset of balding.

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Approximately one year after the devolution of testosterone assays from the SAS, the Analytical Methods Working Party of the Association of Clinical Biochemists set up a working party to investigate the performance of the assays, to survey the available methodology and to give guidance on the factors that influence the assay. This document represents a summary of the deliberations of the group and forms one of a series of similar reports.

An assay for the measurement of 18-hydroxycorticosterone (18-OHB) in plasma has been validated. The method involves extraction of plasma with dichloromethane, thin layer chromatography and radioimmunoassay with an iodinated 18-hydroxycorticosterone-3-carboxymethyloxime ligand. The plasma concentration of 18-OHB was measured in 16 patients with primary hyperaldosteronism and 20 control subjects. After overnight recumbency a significantly higher mean concentration of 18-OHB was found in the samples taken from the patients than in those from the control subjects. The degree of elevation did not clearly discriminate between patients with a unilateral adenoma and those with bilateral adrenal hyperplasia. A significant anomalous postural decrease in the 18-OHB concentration occurred in 10 of the 13 patients with an adenoma, whereas there was a significant postural increase in the three patients with hyperplasia.

To ascertain the use being made of a Supraregional Assay Service laboratory in the diagnosis of primary hyperaldosteronism, follow-up data were obtained on 60 patients in whom the diagnosis was suggested by the biochemical results. In 36 patients an adrenal adenoma had been removed; 14 patients had evidence of an adenoma on CT scan; 10 patients were presumed to have bilateral adrenal hyperplasia. The data used to make the diagnosis of primary hyperaldosteronism and to assess the likelihood of the presence of an adenoma indicate that patients studied at 40 centres in the UK show results very similar to those of North American series where large numbers of patients have been described but all have been studied in the same centre. The majority of patients in our series were treated at the hospital at which the diagnosis was made, thus avoiding referral to a centre distant from the patient's home and indicating that the service was being used as originally intended when the Supraregional Assay Service was set up.